Our broad objective is to understand inducible cellular responses to DNA damage by carcinogens, many of which are mutagens in bacteria, which special emphasis on understanding the relationship between those responses which contribute to cellular survival following carcinogenic damage and those which affect mutagenesis. We use E. coli as a model cell system in which to study inducible SOS responses and adaptive responses, evidence for both of which has also been found in mammalian cells, because of the advantage of availability of relevant mutants and extensive biochemical and genetic characterization. Immediate research objectives include: (1) Factors involved in inducible repair of UV damage and characterization of its mechanism. Having shown that the primary process resulting in enhanced cellular survival and Weigle reactivation by SOS induction is uvr+-dependent and correlates with long patch repair, we are attempting to identify which induced gene products are required and in what capacity. We are also investigating the detailed mechanism of the process to determine whether lesion removal is involved or whether an incision-initiated event which contributes to tolerance of persistent damage is responsible. (2) Substrate for long patch repair of UV damage. Having obtained evidence suggesting that long patches occur at some particular small class of damage sites which are refractory to constitutive repair and which are apparently potent blocks to replication, we are investigating the nature of these sites as an approach to understanding the means by which the inducible process contributes to survival. We are particularly interested in the possibility that lesions in some functionally distinct region of the genome, perhaps growing point regions, are involved. (3) Inducible repair of alkylation damage. Having found that inducible repair synthesis of the long patch type occurs after MNNG damage as it does after UV, we are exploring the extent to which this represents an overlap between the two known inducible processes, the SOS and the adaptive responses, and the means by which it contributes to survival of alkylation damage.